A new clinical trial at the James is pioneering the use of telemedicine to create better treatment options for patients with a rare form of pancreatic cancer. “This is the first nationwide telemedicine therapeutic clinical trial for cancer,” said Sameek Roychowdhury, MD, PhD, a physician scientist and leader in creating innovative ways to look at, understand and treat cancer. “It’s a new way of thinking and providing access to clinical trials.” Roychowdhury and his team at the James identified the fibroblast growth factor receptor (FGFR) gene and how “using a smart drug we could turn it off and slow the cancer growth” it caused. A traditional clinical trial using the smart drug showed promising results in patients with pancreatic cancer and the FGFR gene. Because this was a rare type of cancer, a national clinical trial would be costly.  “How do we give patients access to this?” Roychowdhury said. The answer came during the COVID pandemic and the increased use of telemedicine. “That allowed us to connect the dots and utilize telemedicine,” he said. After a lengthy regulatory and approval process that created a well-thought out and workable plan, the clinical trial began in May. Patients identified with pancreatic cancer and the FGFR gene will be able to remain at home and coordinate their treatment with their local oncologists and Roychowdhury and his team, who will work in tandem. “Instead of a clinical trial in 50 locations and a $20 million price tag, we’ve reduced the cost to $2 million,” he said. Roychowdhury believes this clinical trial will lead to others for rare cancers and make it more cost effective for pharmaceutical companies to create smart drugs for rare forms of cancer. He is working to create a national alliance of oncologists to share ideas, best practices and create more telemedicine clinical trials for rare types of cancers that would otherwise never be opened. “We have identified seven more targets and clinical trials [here at the James],” Roychowdhury said.

Episode 193: The Nation's First Telemedicine Cancer Clinical Trial, with Dr. Sameek Roychowdhury

BUFFALO, NY — August 11, 2025 — Aging (Aging-US) is proud to support a milestone event for the global senescence and aging research community.

This coming September 16-19, 2025, Rome, Italy will host two back-to-back events that will define the next chapter of senescence science and translation:

-10th Annual International Cell Senescence Association (ICSA) Conference
-Senotherapeutics Summit – organized with the Phaedon Institute

This combined program could not come at a more important time. The field is entering a transformative phase:

-Multiple clinical trials on senolytics and senomorphics are now reporting results, offering the first real-world evidence of their therapeutic potential.

-Exciting new discoveries in senescence mechanisms, biomarkers, and tissue-specific roles are reshaping our understanding of when and how to target these cells.

For the first time, the leading fundamental science meeting on cellular senescence will be directly connected with a global summit dedicated to the clinical and commercial development of senotherapeutics. This unique integration will allow participants to seamlessly move from bench to bedside discussions, exploring both the latest research and its translation into therapies that could transform how we approach aging and age-related diseases.

Highlights include:

-Keynotes from pioneers driving both discovery science and translational innovation

-Sessions on mechanisms, biomarkers, and emerging targets

-Industry and regulatory panels on clinical trial design, safety, and approval pathways

-Case studies from ongoing and completed human trials

-Networking with leaders from academia, biotech and pharma

Celebrate a decade of ICSA and help chart the path for the next generation of senescence science and therapeutics.

Registration is still open: https://icsa2025rome.com/

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Aging (Aging-US)

Aging-US Supports Landmark Senescence and Aging Research Events in Rome

Aging (Aging-US) Supports Landmark Senescence and Aging Research Events in Rome

In this special summer episode, Brandon Nappi interviews The Rev’d Adrian Dannhauser, Rector of Church of the Incarnation in New York City and author of Ask Me for a Blessing (You Know You Need One). Adrian and Brandon dive into spiritual call and spiritual practice—from silent retreats to evangelism to the spiritual courage it takes to pray for others who may (or may not) ask for it. Host: Brandon Nappi Guest: Adrian Dannhauser Production: Goodchild Media Music: Wayfaring Stranger, Theodicy Jazz Collective Art: E. Landino Instagram: @theleadersway.podcast berkeleydivinity.yale.edu/podcast You can support our work at https://tinyurl.com/support-transforming-leaders

60: Tell Me About Your Spiritual Side with Adrian Dannhauser

Andrew McGowan, Dean of Berkeley Divinity School and Professor at Yale Divinity School, discusses the origins of today's Christian practices, which Christian rituals were lost over the centuries, and why the famous biblical story of Abraham and Isaac is about trust, not sacrifice.

What We Lost from Early Christianity with Dean Andrew McGowan

In this episode, we go behind the scenes with Reem and Adriana, the deputy editors who led the Yale Journal of Biology and Medicine's special issue on Epigenetics. Our hosts Isha and Delyar discuss the editors’ experience in facing new frontiers in scientific publishing, including developing protocols to detect AI-generated content and ensuring manuscripts contribute meaningfully to the scientific consensus.

Read the “Epigenetics” issue: https://medicine.yale.edu/news-article/explore-yjbms-june-2025-issue-on-epigenetics/

Read more about YJBM at:
https://medicine.yale.edu/yjbm/ 

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YJBM Epigenetics: Interview with Deputy Editors

BUFFALO, NY – August 11, 2025 – A new #researchpaper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.”

In this study, researchers led by first author Aiden Deacon and corresponding author Justin Hwang from the University of Minnesota-Twin Cities investigated a group of genes known as the R-spondin family (RSPO1/2/3/4) in advanced prostate cancer (PC). The RSPO gene family regulates Wnt signaling, a pathway involved in cancer progression.

Prostate cancer is the most common cancer among men in the United States and becomes especially dangerous when it spreads beyond the prostate. Most patients are treated with hormone therapies that target the androgen receptor; however, many tumors eventually become resistant.

The research team analyzed thousands of tumor samples and found that RSPO2 alterations were more common than changes in other R-spondin genes or even some well-known cancer-related genes like CTNNB1 and APC. RSPO2 amplification occurred in over 20% of metastatic prostate cancer. Patients with these alterations showed signs of more aggressive disease, including higher mutation rates and greater tumor complexity.

Using laboratory models, the team discovered that RSPO2 increases cancer cell growth and triggers a biological process called epithelial-mesenchymal transition (EMT). EMT is known to promote tumor spread and resistance to standard treatments. Unlike other genes in the same pathway, RSPO2 also appeared to reduce the activity of androgen receptor genes, suggesting it drives a type of prostate cancer that no longer relies on hormones for growth.

“In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1.”

Importantly, RSPO2 showed structural differences from other R-spondin proteins, which may allow researchers to design drugs that specifically block its activity. Current therapies targeting the Wnt pathway are limited, and there are no approved drugs that inhibit RSPO2. However, this study highlights RSPO2 as a promising therapeutic target, especially for patients who do not respond to existing hormone-based treatments.

This research adds critical knowledge about how aggressive prostate cancers develop and persist despite therapy. The identification of RSPO2 as a key driver of disease progression opens new possibilities for treatment strategies aimed at improving outcomes for patients with advanced prostate cancer.

DOI - https://doi.org/10.18632/oncotarget.28758

Correspondence to - Justin Hwang - jhwang@umn.edu

Video short - https://www.youtube.com/watch?v=iyu5D_c1dbY

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Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics

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Oncotarget

New Gene Linked to Aggressive, Treatment-Resistant Prostate Cancer

Lung cancer, particularly non-small cell lung cancer (NSCLC), is the deadliest cancer worldwide. Cigarette smoking is one of the main causes, but not every smoker develops the disease. This suggests that other biological factors help determine who develops cancer.

Researchers from the Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Indianapolis, and from the Richard L. Roudebush Veterans Affairs Medical Center have now found that cigarette smoke, combined with a weakened DNA repair system, can trigger the early stages of lung cancer, particularly NSCLC. This work, led by first author Nawar Al Nasralla and corresponding author Catherine R. Sears, was recently published in Volume 16 of Oncotarget.

Full blog - https://www.oncotarget.org/2025/08/11/cigarette-smoke-and-weak-dna-repair-a-double-hit-behind-lung-cancer-risk/

Paper DOI - https://doi.org/10.18632/oncotarget.28724

Correspondence to - Catherine R. Sears - crufatto@iu.edu

Video short - https://www.youtube.com/watch?v=UEiCz834a8c

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Keywords - cancer, DNA repair, DNA damage, lung adenocarcinoma, squamous cell carcinoma, Xeroderma Pigmentosum Group C (XPC)

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Cigarette Smoke and Weak DNA Repair: A Double Hit Behind Lung Cancer Risk

BUFFALO, NY — August 12, 2025 — A new #research perspective was #published in Aging (Aging-US) on July 8, 2025, titled “Exercise as a geroprotector: focusing on epigenetic aging.”

In this perspective, led by Takuji Kawamura from Tohoku University, researchers reviewed existing evidence from scientific studies showing that regular exercise, physical activity, and fitness may influence epigenetic aging and potentially reverse it, offering a promising way to extend healthspan and improve long-term health.

Epigenetic aging refers to changes in the body’s DNA that reflect how quickly a person is aging at the molecular level. It is measured using epigenetic clocks, which analyze patterns of DNA methylation, a chemical modification that can affect gene activity. Unlike chronological age, which simply counts the number of years lived, epigenetic aging presents a more accurate picture of how well the body’s cells and tissues are functioning. This process is influenced by various factors, including lifestyle, and has become a powerful tool for studying aging.

This perspective highlights that while general physical activity, such as walking or doing household tasks, offers health benefits, structured exercise routines that are planned, repetitive, and goal-directed appear to have stronger effects on slowing epigenetic aging. Physical fitness, especially high cardiorespiratory capacity, is also closely associated with slower epigenetic aging.

The authors also discuss key findings from both human and animal studies. In mice, structured endurance and resistance training reduced age-related molecular changes in muscle tissue. In humans, multi-week exercise interventions demonstrated reductions in biological age markers in blood and skeletal muscle. One study found that sedentary middle-aged women reduced their epigenetic age by two years after just eight weeks of combined aerobic and strength training. Another study showed that older men with higher oxygen uptake levels, a key measure of cardiovascular fitness, had significantly slower epigenetic aging.

“These findings suggest that maintaining physical fitness delays epigenetic aging in multiple organs and supports the notion that exercise as a geroprotector confers benefits to various organs.”

The research also examines which organs benefit most from exercise. While skeletal muscle has been a central focus, new evidence shows that regular physical training may also slow aging in the heart, liver, fat tissue, and even the gut. In addition, Olympic athletes were found to have slower epigenetic aging than non-athletes, suggesting that long-term, intensive physical activity may have lasting anti-aging effects.

The authors call for further research to understand why some individuals respond more strongly to exercise than others and how different types of training influence aging in various organs. They also point out the importance of developing personalized exercise programs to maximize anti-aging benefits. Overall, the findings support the growing recognition that maintaining physical fitness is not only essential for daily health but may also serve as one of the most effective tools for slowing the body’s internal aging process.

DOI - https://doi.org/10.18632/aging.206278

Corresponding author - Takuji Kawamura - takuji.kawamura.b8@tohoku.ac.jp

Video short - https://www.youtube.com/watch?v=Wro3_wBovdE

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Exercise May Slow Epigenetic Aging

BUFFALO, NY - August 13, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 29, 2025, titled “PCAIs stimulate MAPK, PI3K/AKT pathways and ROS-Mediated apoptosis in aromatase inhibitor-resistant breast cancer cells while disrupting actin filaments and focal adhesion.”

In this study, led by first author Jassy Mary S. Lazarte and corresponding author Nazarius S. Lamango from Florida A&M University College of Pharmacy and Pharmaceutical Sciences, researchers investigated a new class of compounds called polyisoprenylated cysteinyl amide inhibitors (PCAIs) as a potential treatment for aromatase inhibitor (AI) therapy resistant breast cancer. Aromatase inhibitors are a common treatment for estrogen receptor-positive (ER+) breast cancer, but many patients eventually develop resistance, leaving fewer therapeutic options.

The study focused on a PCAI compound called NSL-YHJ-2-27, which was tested in long-term letrozole-treated breast cancer cells (LTLT-Ca), an experimental model of AI therapy resistance. NSL-YHJ-2-27 activated two major signaling pathways, MAPK and PI3K/AKT. Although these pathways typically support cancer cell survival, their overstimulation by PCAIs led to increased oxidative stress, damaging the cells and inducing cell death by apoptosis. The compound also reduced levels of RAC1 and CDC42, proteins involved in maintaining cell shape and movement. These alterations resulted in cytoskeletal disruption and reduced structural integrity, making the cancer cells more vulnerable and less capable of spreading. Importantly, the effects of NSL-YHJ-2-27 persisted after the compound was removed, suggesting long-term control over AI resistant cancer cells may be possible.

“PCAIs inhibited cell proliferation and colony formation by 95% and 74%, respectively, increased active caspase 7 and BAX 1.5-fold and 56%, respectively. NSL-YHJ-2-27 (10 μM) induced LTLT-Ca spheroid degeneration by 61%.”

As a new class of targeted molecules, PCAIs represent an innovative approach distinct from traditional endocrine therapies. Their ability to affect multiple cellular mechanisms simultaneously makes them promising candidates for future drug development.

Overall, this study presents a promising new approach for treating AI therapy-resistant breast cancer. By targeting cellular pathways that support survival and mobility, PCAIs like NSL-YHJ-2-27 could provide a novel strategy to manage advanced or resistant forms of the disease. Further research, including in vivo studies and clinical trials, will be essential to confirm these findings and evaluate their therapeutic potential.

DOI - https://doi.org/10.18632/oncotarget.28759

Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu

Video short - https://www.youtube.com/watch?v=8xQEilloO9Q

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Keywords - cancer, PCAIs, ROS, MAPK, PI3K/AKT, LTLT-Ca cells

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New Compound Disrupts Survival Pathways in Aromatase Inhibitor-Resistant Breast Cancer Cells

BUFFALO, NY — August 14, 2025 — A new #research paper was #published in Volume 17, Issue 7, of Aging (Aging-US) on July 3, 2025, titled “Frailty associates with respiratory exacerbations and mortality in the COPDGene cohort.”

In this study, led by first author Eleanor Kate Phillips from Brigham and Women’s Hospital and corresponding author Dawn L. DeMeo from Brigham and Women’s Hospital and Harvard Medical School, researchers investigated how frailty impacts lung health and survival in individuals with a history of cigarette smoking. They found that frailty raises the risk of lung attacks and death, even in smokers with preserved lung function. This result shows why all current and former smokers should be checked for frailty.

Frailty is a condition that makes the body more vulnerable to illness, especially in older adults. This study focused on more than 2,600 adults with a history of heavy smoking, many of whom showed no signs of lung damage on standard tests. At the second follow-up visit, participants were categorized as robust, prefrail, or frail and followed for about three years. Researchers tracked how often they experienced respiratory attacks, such as episodes of severe coughing or breathlessness, and whether they survived during that period.

“COPDGene is a cohort study of individuals aged 45–80 with a minimum 10 pack-year smoking history.”

The results showed that people who were frail had a three- to five-fold higher chance of developing serious or frequent respiratory attacks compared to those who were robust. These risks were not limited to people with chronic lung disease. In fact, many frail participants with normal lung function still faced a significantly higher chance of lung attacks and death. Even those in the “prefrail” stage, a milder form of frailty, were more likely to experience health complications.

The research team also found that frailty was associated with an accelerated pace of biological aging, measured using a DNA-based test called DunedinPACE. This supports the idea that frailty may reflect deeper biological changes in the body that go beyond what traditional lung function tests can detect. These findings challenge the idea that standard lung tests can rule out future respiratory complications in people with a history of smoking. 

Altogether, the study shows that simple frailty checks could help identify early health problems, allowing for timely interventions that may prevent hospitalizations and potentially save lives. The study suggests that frailty screening may be a valuable tool in public health efforts to reduce respiratory disease and improve outcomes for aging adults.

DOI - https://doi.org/10.18632/aging.206275

Corresponding author - Dawn L. DeMeo - redld@channing.harvard.edu

Video short - https://www.youtube.com/watch?v=G1XQhQN6PQ8

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Keywords - aging, frailty, cigarette smoking, respiratory exacerbations, COPD, epigenetic aging

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Frailty Linked to Higher Risk of Respiratory Complications and Death in Smokers

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

New Compound Disrupts Survival Pathways in Aromatase Inhibitor-Resistant Breast Cancer Cells

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